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J S Denton

Publications and source records attributed to J S Denton.

9 recordsLinked to original sources
PubMed2000

Homicidal commotio cordis in two children.

This paper's objective is to describe two cases of fatal commotio cordis resulting from the deliberate striking of children's chests by adults with their fists. These deaths involve two male children, ages 3 years and 14 months. The clinical histories, events in the households prior to the deaths, behaviors of the children, autopsy findings, and investigation results are all similar. In both cases, fatal blows were delivered to the anterior chest with a closed fist. Both children collapsed immediately, unable to be resuscitated. Confessions were obtained in both cases by investigators soon after the children's deaths. Autopsies showed chest contusions in only one child, presumably due to knuckle impact. The cardiac rhythms noted by paramedics were ventricular fibrillation and asystole. Due to the lack of physical findings, an immediate and thorough investigation is critical. An accurate history of events preceding death must be obtained.

Child Abuse↗
PubMed1999

The NH(2) terminus of the epithelial sodium channel contains an endocytic motif.

An epithelial sodium channel (ENaC) is composed of three homologous subunits: alpha, beta, and gamma. To elucidate the function of the cytoplasmic, NH(2) terminus of rat ENaC (rENaC) subunits, a series of mutant cDNAs was constructed and the cRNAs for all three subunits were expressed in Xenopus oocytes. Amiloride-sensitive Na(+) currents (I(Na)) were measured by the two-electrode voltage clamp technique. Deletion of the cytoplasmic, NH(2) terminus of alpha (Delta2-109), beta (Delta2-49), or gamma-rENaC (Delta2-53) dramatically reduced I(Na). A series of progressive, NH(2)-terminal deletions of alpha-rENaC were constructed to identify motifs that regulate I(Na). Deletion of amino acids 2-46 had no effect on I(Na): however, deletion of amino acids 2-51, 2-55, 2-58, and 2-67 increased I(Na) by approximately 4-fold. By contrast, deletion of amino acids 2-79, 2-89, 2-100, and 2-109 eliminated I(Na). To evaluate the mechanism whereby Delta2-67-alpha-rENaC increased I(Na), single channels were evaluated by patch clamp. The single-channel conductance and open probability of alpha,beta,gamma-rENaC and Delta2-67-alpha,beta,gamma-rENaC were similar. However, the number of active channels in the membrane increased from 6 +/- 1 channels per patch with alpha,beta,gamma-rENaC to 11 +/- 1 channels per patch with Delta2-67-alpha,beta,gamma-rENaC. Laser scanning confocal microscopy confirmed that there were more Delta2-67-alpha,beta, gamma-rENaC channels in the plasma membrane than alpha,beta, gamma-rENaC channels. Deletion of amino acids 2-67 in alpha-rENaC reduced the endocytic retrieval of channels from the plasma membrane and increased the half-life of the channel in the membrane from 1.1 +/- 0.2 to 3.5 +/- 1.1 h. We conclude that the cytoplasmic, NH(2) terminus of alpha-, beta-, and gamma-rENaC is required for channel activity. The cytoplasmic, NH(2) terminus of alpha-rENaC contains two key motifs. One motif regulates the endocytic retrieval of the channel from the plasma membrane. The second motif is required for channel activity.

Amiloride↗
PubMed1999

Esophagoaortic perforation by foreign body (coin) causing sudden death in a 3-year-old child.

We report an extremely unusual consequence to foreign body ingestion in a case of a 3-year-old boy who died suddenly and at autopsy was found to have an esophagoaortic fistula. This fistula was caused by a coin which lodged posteriorly and eroded through the esophagus into the aorta. Serious complications following foreign body ingestion are rare and include stricture formation, intramural abscess, and the formation of fistula tracts. This case illustrates the potentially unpredictable behavior of impacted foreign bodies. The child's parents were initially suspected of child abuse based on the terminal hemoptysis.

Aorta↗
PubMed1999

Intracellular H+ regulates the alpha-subunit of ENaC, the epithelial Na+ channel.

Protons regulate electrogenic sodium absorption in a variety of epithelia, including the cortical collecting duct, frog skin, and urinary bladder. Recently, three subunits (alpha, beta, gamma) coding for the epithelial sodium channel (ENaC) were cloned. However, it is not known whether pH regulates Na+ channels directly by interacting with one of the three ENaC subunits or indirectly by interacting with a regulatory protein. As a first step to identifying the molecular mechanisms of proton-mediated regulation of apical membrane Na+ permeability in epithelia, we examined the effect of pH on the biophysical properties of ENaC. To this end, we expressed various combinations of alpha-, beta-, and gamma-subunits of ENaC in Xenopus oocytes and studied ENaC currents by the two-electrode voltage-clamp and patch-clamp techniques. In addition, the effect of pH on the alpha-ENaC subunit was examined in planar lipid bilayers. We report that alpha,beta,gamma-ENaC currents were regulated by changes in intracellular pH (pHi) but not by changes in extracellular pH (pHo). Acidification reduced and alkalization increased channel activity by a voltage-independent mechanism. Moreover, a reduction of pHi reduced single-channel open probability, reduced single-channel open time, and increased single-channel closed time without altering single-channel conductance. Acidification of the cytoplasmic solution also inhibited alpha, beta-ENaC, alpha,gamma-ENaC, and alpha-ENaC currents. We conclude that pHi but not pHo regulates ENaC and that the alpha-ENaC subunit is regulated directly by pHi.

Acids↗
PubMed1997

Noncirrhotic portal vein thrombosis causing sudden unexpected death. A rare cause of fatally ruptured esophageal varices.

Noncirrhotic portal vein thrombosis (PVT) is a rare disease that usually presents with small nonfatal "herald bleeding" with low mortality. Classic findings of noncirrhotic PVT include esophageal varices, splenomegaly, a normal liver, and an organized thrombus of the portal vein. We present a case of previously unreported sudden unexpected death from noncirrhotic PVT in an asymptomatic elderly woman, review the literature of this entity, and examine the pathophysiology of the formation of fatally ruptured varices. The portal vein must be carefully examined in all cases where there is no coexisting cirrhosis.

Aged↗
PubMed1988

A (2'-5')An-dependent endonuclease: tissue distribution in BALB/c mice and the effects of IFN-beta treatment and anti-IFN-alpha/beta immunoglobulin on the levels of the enzyme.

A (2'-5')oligoadenylate-dependent endoribonuclease (RNase L) is an important mediator of the IFN-induced antiviral state. RNase L has been found in several different murine tissues at levels comparable to those previously observed in cultured cells. A basal level of RNase L is present in all tissues assayed. The levels of RNase L in tissues are not significantly increased in mice following treatment with interferon-beta (IFN-beta). The amount of RNase L is, however, decreased in spleen when mice are injected with rabbit antimouse IFN-alpha/beta immunoglobulin. These data suggest that relatively high levels of RNase L may be maintained in tissues by endogenous IFN-alpha/beta production.

Animals↗
PubMed1988

Age-dependent changes are observed in the levels of an enzyme mediator of interferon action: a (2'-5')A(n)-dependent endoribonuclease.

A (2'-5')oligoadenylate-dependent endoribonuclease (RNase L) is an important mediator of interferon's antiviral actions. Levels of this enzyme were determined in spleen, lung, liver, and kidney of mice at different times after birth. The levels of RNase L were found to be relatively low in newborn kidney, lung, and spleen. RNase L levels rise 2- to 10-fold in these three tissues as mice approach 5 days of age. In the spleen, levels of RNase L remain high as mice reach adult life. In the lung and kidney, however, RNase L levels decrease after 14 days. RNase L levels in the liver are highest from birth to 5-7 days and then decrease subsequently and remain low in adult mice. These changes in RNase L levels with postnatal development may be important with regard to age-specific susceptibility to some virus infections.

Aging↗